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Objective: To document blood nitric oxide concentrations in the portal vein and systemic circulation in a rat model of acute portal hypertension and compare values with a control group and a sham surgical group., Animals: 30 rats; 10 controls (group 1), 10 sham surgical (group 2), and 10 rats with surgically induced acute portal hypertension (group 3)., Procedure: Following induction of anesthesia, catheters were placed surgically in the carotid artery, jugular, and portal veins of group 2 and 3 rats and in the carotid artery and jugular vein of group 1 rats. Baseline heart and respiratory rates, rectal temperature, and vascular pressure measurements were obtained, and blood was drawn from all catheters for baseline nitric oxide (NO) concentrations. Acute portal hypertension was induced in the group 3 rats by tying a partially occluding suture around the portal vein and a 22-gauge catheter. The catheter was then removed, resulting in a repeatable degree of portal vein impingement. After catheter placement, all variables were remeasured at 15-minute intervals for 3 hours., Results: Blood nitric oxide concentrations were greater in all vessels tested in group 3 than in group 2 rats., Conclusions and Clinical Relevance: Acute portal hypertension in this experimental model results in increased concentrations of NO in the systemic and portal circulation. On the basis of information in the rat, it is possible that increased NO concentrations may develop in dogs following surgical treatment of congenital portosystemic shunts if acute life-threatening portal hypertension develops. Increased NO concentrations may contribute to the shock syndrome that develops in these dogs.

Objective: To determine existence of portal and systemic bacteremia in dogs with induced severe hepatic disease, compared with clinically normal dogs, before and after vena caval banding., Animals: 6 control dogs and 10 dogs with induced severe hepatic disease and multiple portosystemic shunts (PSS)., Procedure: Dogs of the diseased group were given dimethylnitrosamine (2 mg/kg of body weight, PO) twice weekly until multiple PSS developed. Surgery was performed on dogs of both groups, and blood for baseline aerobic and anaerobic bacterial culture was collected from catheters placed in the portal and hepatic veins and caudal vena cava. All dogs underwent vena caval banding, and blood for aerobic and anaerobic bacterial culture was collected from the portal and hepatic venous catheters at 120, 240, and 360 minutes after banding., Results: Compared with control dogs (16% gram-positive and 84% gram-negative bacteria), diseased dogs had significantly higher percentage of gram-positive bacteria (42% of positive culture results, P < or = 0.01) and significantly lower percentage of gram-negative bacteria (58% of positive culture results, P < or = 0.01) isolated. Pseudomonas aeruginosa was isolated most frequently from dogs of both groups; more than 1 organism was isolated from 5 dogs of each group. Antimicrobial susceptibility included that to aminoglycosides (particularly amikacin), fluorinated quinolones, and imipenem., Conclusion: Portal and systemic, predominantly gram-negative, bacteremia is present in catheterized, clinically normal dogs and dogs with dimethylnitrosamine-induced hepatic disease and multiple PSS.

Objective: To document presence of endotoxin in portal and systemic blood in a model of canine multiple portosystemic shunts (PSS), and compare values in clinically normal dogs, before and after vena caval banding., Animals: 6 control dogs and 10 dogs with dimethylnitrosamine-induced multiple PSS that were subjected to vena caval banding., Procedure: Dimethylnitrosamine was administered orally (2 mg/kg of body weight, twice weekly) to the 10 dogs in the diseased group until multiple PSS developed. Surgery was then performed on all 16 dogs (both groups), and shunts were confirmed in the diseased dogs. Blood was collected from the portal vein, hepatic vein, and caudal vena cava baseline endotoxin determination and aerobic and anaerobic blood culturing. Baseline pressure measurements were taken from the portal venous catheter; then vena caval banding was performed. Blood for endotoxin determinations was taken from all vessels 20, 40, 60, 120, 240, and 360 minutes after banding; portal pressure measurements were taken at the same time as sample acquisition. Blood for culturing was taken from the portal and hepatic venous catheters at 120, 240, and 360 minutes after banding., Results: Dogs in the diseased group had significantly greater overall presence of endotoxin in the portal vein (P < or = 0.0002), hepatic vein (P < or = 0.0001), and caudal vena cava (P < or = 0.0004) than did control dogs. With respect to time, endotoxin presence was greater in the diseased group before banding (P < or = 0.0002), and at 20 (P < or = 0.0008), 40 (P < or = 0.002), 60 (P < or = 0.006), and 120 (P < or = 0.01) minutes after banding., Conclusions: Endotoxemia is more frequently present in catheterized dogs with dimethylnitrosamine-induced hepatic disease and multiple PSS, compared with clinically normal dogs. Additionally, portal pressure changes induced by vena caval banding did not affect endotoxemia., Clinical Relevance: Endotoxemia may exist in dogs with hepatic disease and multiple PSS, and should be kept in mind when formulating treatment (particularly antimicrobial selection) for dogs with suspected endotoxemia.

To measure tracheal mucociliary transport rate (TMTR) in awake dogs, restrained in dorsal recumbency, 99mtechnetium-labeled macroaggregated albumin was administered by tracheal injection, and the cephalic movement of boluses containing the radiopharmaceutical was detected by a gamma camera positioned lateral to the dog's head and neck. The distance traveled by each bolus was measured, relative to external markers placed a known distance apart. Tracheal mucociliary transport rates were calculated by dividing the measured distance of radiopharmaceutical movement by elapsed time. The technique was efficient and well tolerated. Mean (+/- SD) TMTR was 35.3 +/- 15.9 mm/min. Significant (P = 0.029) difference in TMTR was found between males and females, but significant difference attributable to age of the dog was not detected. This method of measuring TMTR in awake dogs has potential for evaluation of clinical animal patients with suspected tracheal mucociliary abnormalities.

Effects of vena caval banding on portal venous and vena caval hemodynamics were examined in 6 control dogs and in 10 dogs that had undergone attenuation (banding) of the abdominal part of the caudal vena cava and had dimethylnitrosamine-induced multiple portosystemic shunts (PSS). Additionally, indocyanine green (ICG) extraction and clearance after infusion to steady state were used to calculate hepatic plasma flow in these dogs. Sixteen dogs were randomly assigned to 2 groups: control (n = 6) or diseased (n = 10). Diseased dogs were administered dimethylnitrosamine (2 mg/kg, PO, twice weekly) until multiple PSS developed, as assessed by results of clinical laboratory tests, ultrasonography, and hepatic scintigraphy. Shunts were confirmed visually at celiotomy and by contrast portography. Venous pressures (caudal vena caval, portal, and hepatic) were recorded before and after vena caval banding for up to 7 days in dogs from both groups. Peritoneal cavity pressures were recorded in all dogs after closure of the body wall. To determine ICG extraction and clearance, a bolus injection of ICG (0.5 mg/kg, i.v.) was administered, followed by steady-state infusion of 0.097 mg/min. Extractions and clearances of ICG were measured, and from these, hepatic plasma flow rates were determined immediately before and after banding and at 6 hours, 48 hours, and 7 days after banding. The gradient (caudal vena caval pressure within 1 to 2 mm of Hg of portal pressure) between caudal vena cava and portal venous pressures established at banding was maintained after the first hour in both groups. Caudal vena cava pressures established at banding were maintained throughout the study, with the exception of the first hour in diseased dogs. Extraction ratios were higher in control dogs at all times, except at 48 hours. Clearance was higher in control dogs at all times. Hepatic plasma flow did not differ between groups, except immediately after banding, when flow was greater in diseased dogs, and differences were not found over time in either group. This study indicated that vena caval banding in this model of experimentally induced multiple PSS increases and maintains caudal vena cava pressure, relative to portal venous pressure (after the first hour) for 7 days, and that calculated hepatic plasma flow is not persistently improved by vena caval banding.

Comparison was made of the healing of sutured prescrotal urethral incisions (12 dogs) with that of nonsutured incisions (6 dogs). Comparison was also made of the healing of 5-0 polyglactin 910-sutured urethral incisions (6 dogs) with that of 5-0 polydioxanone-sutured incisions (6 dogs). Three dogs from each treatment group were euthanatized 3 weeks and 6 weeks after the surgical procedure. Surgical sites were examined grossly, and urethral circumference measurements were taken at 3 locations (surgical site, 1 cm cranially, and 1 cm caudally). Transverse sections of the surgical sites were prepared and examined by light microscopy. Hemorrhage occurred postoperatively in dogs in which the incisions were not sutured. The surgical sites from the 6 dogs in which incisions healed by second intention had more fibrosis and less inflammation than did those that were sutured. There was little difference between incisions sutured with polyglactin 910 and those sutured with polydioxanone suture material. Postoperative urethral stricture formation did not occur in any of the dogs.